SLC38A2 and breast carcinoma: Considering the heterogeneity of response to the stresses, here we assessed the route of SLC38A2 degradation by treating MCF7, MDA-MB-231 and HCC1806 with Bafilomycin A1, a pharmacological inhibitor of autophagosome-lysosome fusion.28 The levels of SLC38A2 increased consistently after Bafilomycin A1 treatment in all cell lines, suggesting lysosome-mediated degradation of SLC38A2 was also important in these breast cancer cell lines (Fig. 3a).